Cd300a, an inhibitory receptor, belongs to the CD300 family of cell surface molecules. Its inhibitory signal depends on tyrosine residue phosphorylation in ITIMs of the cytoplasmic tail. Cd300a is broadly expressed on myeloid and lymphoid cells, regulating diverse immune cell processes. It recognizes phosphatidylserine and phosphatidylethanolamine, influencing immune functions and the host response to diseases [3].

In KO mouse models, Cd300a -/- mice showed ameliorated neurological deficit after middle cerebral artery occlusion as Cd300a inhibits the CD300b-DAP12 signaling pathway for efferocytosis, and its deficiency enhanced efferocytosis by infiltrating myeloid cells [1]. In allergic inflammation, absence of Cd300a led to increased sensitivity of naïve macrophages to activation and augmented the inflammatory state [2]. In a murine gout model, CD300a -/- mice had persistent neutrophil influx, increased IL-1β, and greater tissue damage due to reduced neutrophil apoptosis [4]. Blocking CD300a in Leishmania-infected mice enhanced early parasite clearance by modulating phagocytic and T-cell effector functions [5].

In conclusion, Cd300a plays a crucial role in regulating immune cell functions, such as efferocytosis, macrophage activation, neutrophil apoptosis, and T-cell differentiation. Studies using Cd300a KO mouse models have revealed its significance in diseases like ischemic stroke, allergic inflammation, gout, and visceral leishmaniasis, providing potential therapeutic targets for these conditions.